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Impact of Gastrointestinal Bacillus anthracis Infection on Hepatic B Cells.

Colliou N, Sahay B, Zadeh M, Owen JL, Mohamadzadeh M - Toxins (Basel) (2015)

Bottom Line: Additionally, despite a global decrease in the B cell population, we observed an increase in both B-1a and marginal zone (MZ)-like B cells.Accumulation of these cells in the liver was associated with an increase in chemokine expression.Further research is required to evaluate the possible cause of their failure to clear the infection within the liver, including the potential role of dysfunctional mitogen-activated protein kinase (MAPK) signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA. collioun@ufl.edu.

ABSTRACT
Ingestion of Bacillus anthracis results in rapid gastrointestinal (GI) infection, known as GI anthrax. We previously showed that during GI anthrax, there is swift deterioration of intestinal barrier function leading to translocation of gut-associated bacteria into systemic circulation. Additionally, we described dysfunction in colonic B cells. In concordance with our previous studies, here, we report early migration of the Sterne strain of B. anthracis along with other gut-resident bacteria into the infected murine liver. Additionally, despite a global decrease in the B cell population, we observed an increase in both B-1a and marginal zone (MZ)-like B cells. Both of these cell types are capable of producing immunoglobulins against common pathogens and commensals, which act as a general antibody barrier before an antigen-specific antibody response. Accumulation of these cells in the liver was associated with an increase in chemokine expression. These data suggest that the presence of Sterne and other commensals in the liver trigger migration of MZ-like B cells from the spleen to the liver to neutralize systemic spread. Further research is required to evaluate the possible cause of their failure to clear the infection within the liver, including the potential role of dysfunctional mitogen-activated protein kinase (MAPK) signaling.

No MeSH data available.


Related in: MedlinePlus

Sterne infection leads to changes in chemokine production in the liver and spleen. A/J mice (n = 43) were infected with 109 spores of B. anthracis Sterne. Total RNA was isolated from mice (day 1, n = 10; day 2, n = 10, day 3, n = 10; day 5 n = 13) at each indicated time point, and transcripts of CXCL10, CXCL11, CXCL12, CXCL13, CXCL16, and CCL25 were evaluated by qRT-PCR, as mentioned in the Experimental Section using gene specific primers. Data are shown as mean ± SEM. *p < 0.05, ** <0.01, ***p < 0.001 compared with PBS-treated or day 0 mice.
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toxins-07-03805-f003: Sterne infection leads to changes in chemokine production in the liver and spleen. A/J mice (n = 43) were infected with 109 spores of B. anthracis Sterne. Total RNA was isolated from mice (day 1, n = 10; day 2, n = 10, day 3, n = 10; day 5 n = 13) at each indicated time point, and transcripts of CXCL10, CXCL11, CXCL12, CXCL13, CXCL16, and CCL25 were evaluated by qRT-PCR, as mentioned in the Experimental Section using gene specific primers. Data are shown as mean ± SEM. *p < 0.05, ** <0.01, ***p < 0.001 compared with PBS-treated or day 0 mice.

Mentions: The chemokines CXCL10; -11; -12; -13; and -16 have been implicated in either B cell trafficking or the infiltration of other immune cells into the liver [23,24,25,26,27]. To evaluate whether expression of these chemokines is altered with Sterne infection; we analyzed transcripts by qRT-PCR; which revealed differential expression of CXCL10; -11; -12; -13; and -16 in the liver and in the spleen during Sterne infection (Figure 3). CXCL10 and -11 (ligands for the CXCR3 receptor) were moderately expressed in the liver; however; their expression was downregulated in the infected spleen. The expression of these two chemokines is dependent upon interferon signaling; they then recruit inflammatory leukocytes to the inflamed loci [28]. It is conceivable that inflammation would be increased with polymicrobial infiltrates; as seen in the liver during Sterne infection. CXCL12 binds to its receptor; CXCR4; and is secreted in response to Toll-like receptor (TLR) and cytokine signaling; to recruit inflammatory leukocytes [29,30]; this chemokine was inhibited during Sterne infection. The classical chemokine for B cell recruitment; CXCL13; was significantly increased during Sterne infection in the liver; however; its expression in the spleen was moderately decreased at day five post-Sterne infection (Figure 3). Perturbation in chemokine expression in the liver and the spleen may form a temporary chemokine gradient for the migration of cells from a distant location; including from the spleen to the liver. Furthermore; the downregulation of homeostatic lymphoid chemokines in the spleen; such as CXCL13; could lead to disruption of the splenic architecture; resulting in the traffic of MZ-like B cells into the liver.


Impact of Gastrointestinal Bacillus anthracis Infection on Hepatic B Cells.

Colliou N, Sahay B, Zadeh M, Owen JL, Mohamadzadeh M - Toxins (Basel) (2015)

Sterne infection leads to changes in chemokine production in the liver and spleen. A/J mice (n = 43) were infected with 109 spores of B. anthracis Sterne. Total RNA was isolated from mice (day 1, n = 10; day 2, n = 10, day 3, n = 10; day 5 n = 13) at each indicated time point, and transcripts of CXCL10, CXCL11, CXCL12, CXCL13, CXCL16, and CCL25 were evaluated by qRT-PCR, as mentioned in the Experimental Section using gene specific primers. Data are shown as mean ± SEM. *p < 0.05, ** <0.01, ***p < 0.001 compared with PBS-treated or day 0 mice.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4591657&req=5

toxins-07-03805-f003: Sterne infection leads to changes in chemokine production in the liver and spleen. A/J mice (n = 43) were infected with 109 spores of B. anthracis Sterne. Total RNA was isolated from mice (day 1, n = 10; day 2, n = 10, day 3, n = 10; day 5 n = 13) at each indicated time point, and transcripts of CXCL10, CXCL11, CXCL12, CXCL13, CXCL16, and CCL25 were evaluated by qRT-PCR, as mentioned in the Experimental Section using gene specific primers. Data are shown as mean ± SEM. *p < 0.05, ** <0.01, ***p < 0.001 compared with PBS-treated or day 0 mice.
Mentions: The chemokines CXCL10; -11; -12; -13; and -16 have been implicated in either B cell trafficking or the infiltration of other immune cells into the liver [23,24,25,26,27]. To evaluate whether expression of these chemokines is altered with Sterne infection; we analyzed transcripts by qRT-PCR; which revealed differential expression of CXCL10; -11; -12; -13; and -16 in the liver and in the spleen during Sterne infection (Figure 3). CXCL10 and -11 (ligands for the CXCR3 receptor) were moderately expressed in the liver; however; their expression was downregulated in the infected spleen. The expression of these two chemokines is dependent upon interferon signaling; they then recruit inflammatory leukocytes to the inflamed loci [28]. It is conceivable that inflammation would be increased with polymicrobial infiltrates; as seen in the liver during Sterne infection. CXCL12 binds to its receptor; CXCR4; and is secreted in response to Toll-like receptor (TLR) and cytokine signaling; to recruit inflammatory leukocytes [29,30]; this chemokine was inhibited during Sterne infection. The classical chemokine for B cell recruitment; CXCL13; was significantly increased during Sterne infection in the liver; however; its expression in the spleen was moderately decreased at day five post-Sterne infection (Figure 3). Perturbation in chemokine expression in the liver and the spleen may form a temporary chemokine gradient for the migration of cells from a distant location; including from the spleen to the liver. Furthermore; the downregulation of homeostatic lymphoid chemokines in the spleen; such as CXCL13; could lead to disruption of the splenic architecture; resulting in the traffic of MZ-like B cells into the liver.

Bottom Line: Additionally, despite a global decrease in the B cell population, we observed an increase in both B-1a and marginal zone (MZ)-like B cells.Accumulation of these cells in the liver was associated with an increase in chemokine expression.Further research is required to evaluate the possible cause of their failure to clear the infection within the liver, including the potential role of dysfunctional mitogen-activated protein kinase (MAPK) signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA. collioun@ufl.edu.

ABSTRACT
Ingestion of Bacillus anthracis results in rapid gastrointestinal (GI) infection, known as GI anthrax. We previously showed that during GI anthrax, there is swift deterioration of intestinal barrier function leading to translocation of gut-associated bacteria into systemic circulation. Additionally, we described dysfunction in colonic B cells. In concordance with our previous studies, here, we report early migration of the Sterne strain of B. anthracis along with other gut-resident bacteria into the infected murine liver. Additionally, despite a global decrease in the B cell population, we observed an increase in both B-1a and marginal zone (MZ)-like B cells. Both of these cell types are capable of producing immunoglobulins against common pathogens and commensals, which act as a general antibody barrier before an antigen-specific antibody response. Accumulation of these cells in the liver was associated with an increase in chemokine expression. These data suggest that the presence of Sterne and other commensals in the liver trigger migration of MZ-like B cells from the spleen to the liver to neutralize systemic spread. Further research is required to evaluate the possible cause of their failure to clear the infection within the liver, including the potential role of dysfunctional mitogen-activated protein kinase (MAPK) signaling.

No MeSH data available.


Related in: MedlinePlus